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Birmingham, AL, United States

The University of Alabama at Birmingham is a public university in Birmingham in the U.S. state of Alabama. Developed from an academic extension center established in 1936, the institution became an autonomous institution in 1969 and is today one of three institutions in the University of Alabama System. In the fall of 2013, 18,568 students from more than 110 countries were enrolled at UAB pursuing studies in 140 programs of study in 12 academic divisions leading to bachelor's, master's, doctoral, and professional degrees in the social and behavioral science, the liberal arts, business, education, engineering, and health-related fields such as medicine, dentistry, optometry, nursing, and public health.The UAB Health System, one of the largest academic medical centers in the United States, is affiliated with the university. UAB Hospital sponsors residency programs in medical specialties, including internal medicine, neurology, surgery, radiology, and anesthesiology. UAB Hospital is the only ACS verified Level I trauma center in Alabama, as rated by the American College of Surgeons Trauma Program.UAB is the state's largest employer, with more than 18,000 faculty and staff and over 53,000 jobs at the university and in the health system. An estimated 10 percent of the jobs in the Birmingham-Hoover Metropolitan Area and 1 in 33 jobs in the state of Alabama are directly or indirectly related to UAB. The university's overall annual economic impact was estimated to be $4.6 billion in 2010. Wikipedia.


Wang J.,University of Alabama at Birmingham
Cold Spring Harbor perspectives in biology | Year: 2012

Wnts are evolutionarily conserved signaling ligands critical for animal development. Genetic engineering in the mouse has enabled investigators to acquire a detailed activation profile of the β-catenin-dependent canonical Wnt pathway during mouse development, and to manipulate Wnt pathway activities with great spatial and temporal precision. Together, these studies have not only revealed important functions of Wnt signaling at multiple stages of early mouse development, but also elucidated how the Wnt pathway interacts with other pathways to form signaling networks that confer the unique features of mammalian embryogenesis. Additionally, the planar cell polarity pathway has emerged as an essential β-catenin independent noncanonical Wnt pathway that coordinates cell polarity and regulates tissue morphogenesis in various mammalian developmental processes. Importantly, studies of Wnt signaling in mouse development have also revealed important pathogenic mechanisms of several congenital disorders in humans. Source


Zhou D.,University of Alabama at Birmingham
Nature genetics | Year: 2010

We show that knockdown of KLF1 in human and mouse adult erythroid progenitors markedly reduces BCL11A levels and increases human gamma-globin/beta-globin expression ratios. These results suggest that KLF1 controls globin gene switching by directly activating beta-globin and indirectly repressing gamma-globin gene expression. Controlled knockdown of KLF1 in adult erythroid progenitors may provide a method to activate fetal hemoglobin expression in individuals with beta-thalassemia or sickle cell disease. Source


Tolwani A.,University of Alabama at Birmingham
New England Journal of Medicine | Year: 2012

Acute limb ischemia due to a perioperative type B (distal) thoracic aortic dissection develops in a 90-kg, 20-year-old man with Marfan's syndrome who is admitted to the hospital for elective aortic-valve replacement. On postoperative day 1, he undergoes endovascular repair of the thoracic aorta. On postoperative day 4, his urine output decreases to 420 ml over a 24-hour period. He requires mechanical ventilation with a fraction of inspired oxygen (FIO2) of 0.70; his mean arterial pressure is 74 mm Hg with vasopressor support. He has had a positive fluid balance of 9.8 liters since admission. The serum creatinine level has increased from a baseline of 0.6 mg per deciliter (53.0 μmol per liter) to 4.4 mg per deciliter (389.0 μmol per liter). The bicarbonate level is 19 mmol per liter despite bicarbonate infusion, and the potassium level is 6.1 mmol per liter. The creatine kinase level has increased to 129,040 U per liter. An intensive care specialist evaluates the patient and recommends initiation of continuous renal-replacement therapy. Copyright © 2012 Massachusetts Medical Society. Source


Calhoun D.A.,University of Alabama at Birmingham
Annual Review of Medicine | Year: 2013

Resistant hypertension affects an estimated 10-15 million American adults and is increasing in prevalence. The etiology of resistant hypertension is almost always multifactorial, including obesity, older age, high dietary salt, chronic kidney disease, and aldosterone excess. Classical primary aldosteronism and lesser degrees of aldosterone excess, possibly originating from visceral adipocytes, contribute broadly to antihypertensive treatment resistance. Treatment of resistant hypertension is predicated on appropriate lifestyle changes and use of effective combinations of antihypertensive agents from different classes. Blockade of aldosterone with spironolactone has been shown to be particularly effective for treatment of resistant hypertension. The antihypertensive benefit of spironolactone is not limited to patients with demonstrable hyperaldosteronism but instead can be effective in resistant hypertensive patients regardless of aldosterone levels. Chlorthalidone is a potent, long-acting thiazide-like diuretic and should be used preferentially to treat resistant hypertension as it is superior to normally used doses of hydrochlorothiazide. Copyright © 2013 by Annual Reviews. Source


Roberson E.D.,University of Alabama at Birmingham
Annals of Neurology | Year: 2012

The pace of discovery in frontotemporal dementia (FTD) has accelerated dramatically with the discovery of new genetic causes and pathological substrates of the disease. MAPT/tau, GRN/progranulin, and C9ORF72 have emerged as common FTD genes, and TARDBP/TDP-43, VCP, FUS, and CHMP2B have been identified as less common genetic causes. TDP-43 and FUS have joined tau as common neuropathological substrates of the disease. Mouse models provide an important tool for understanding the role of these molecules in FTD pathogenesis. Here, we review recent progress with mouse models based on tau, TDP-43, progranulin, VCP, and CHMP2B. We also consider future prospects for FTD models, including developing new models to address unanswered questions. There are also opportunities for capitalizing on conservation of the salience network, which is selectively vulnerable in FTD, and the availability of FTD-related behavioral paradigms to analyze mouse models of the disease. Ann Neurol Copyright © 2012 American Neurological Association. Source

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